Objective:To analyze the risk factors for central venous catheter-associated bloodstream infection in patients with emergency hemorrhagic shock.Methods:Patients with hemorrhagic shock and central venous catheterization admitted to the emergency department of Shanghai First People's Hospital from June 2016 to June 2022 were retrospectively analyzed. The patients were divided into infected group and non-infected group according to whether catheter-related bloodstream infection occurred. The puncture site samples and catheter tip samples of infected patients were collected for etiological detection and drug sensitivity test. The difference of baseline data between the two groups was analyzed, and the relationship between central venous catheter-associated infection and influencing factors was analyzed by multivariate logistic regression.Results:A total of 249 patients were included in this study, including 54 patients in the infected group and 195 patients in the non-infected group. There were significant differences in age, catheterization position, ultrasound-guided puncture, acute physiology and chronic health evaluationⅡ(APACHEⅡ) score, catheter retention time and application of broad-spectrum antibiotics between the infected group and the non-infected group (all P<0.05). Multivariate logistic regression analysis showed that advanced age, femoral vein catheterization, no ultrasound-guided puncture, high APACHEⅡ score, long catheter indent time and application of broad-spectrum antibiotics were risk factors for central venous catheter-associated bloodstream infection. Among the 54 infected patients, Staphylococcus epidermidis accounted for 44.4%, followed by Escherichia coli accounted for 24.1% and fungus accounted for 11.1%. The resistance rate of gram-positive cocci to vancomycin was the lowest (3.4%) followed by tetracycline (34.5%), and the highest resistance rate was amoxicillin (100.0%). The resistance rates of gram-negative bacilli to amikacin and ceftriaxone were relatively high, both of which were 94.7%. Conclusions:The risk factors for central venous catheter-related blood stream infection in patients with emergency hemorrhagic shock included advanced age, femoral vein catheterization, no ultrasound-guided puncture, high APACHEⅡ score, long catheter retention time and use of broad-spectrum antibiotics. The common pathogenic bacteria were Staphylococcus epidermidis and Escherichia coli.

Objective:To investigate the effect of SKF96365, store-operated calcium entry (SOCE) inhibitor, on liver and kidney injury induced by paraquat (PQ).Methods:A549 cells were cultured in vitro and divided into the control group (DMSO group, SKF 2 μmol/L group, and SKF 10 μmol/L group) and PQ group (PQ+DMSO group, PQ+SKF 2 μmol/L group, and PQ+SKF 10 μmol/L group). The nuclear factor of activated T cells (NFAT) in A549 cells was detected by luciferase reporter gene technique. The mouse model of PQ poisoning was constructed and divided into the control group, SKF group, PQ group and PQ+SKF group. In the PQ group, mice were injected with 50 mg/kg PQ intraperitoneally; in the SKF group, mice were injected intraperitoneally with 10 mg/kg SKF96365 for 3 days. Mice in the PQ+SKF group received 50 mg/kg intraperitoneal injection of PQ once and 10 mg/kg intraperitoneal injection of SKF96365 daily for 3 days. On the fourth day, the mice were sacrificed, and the liver and kidney tissues were taken. The histopathological changes of liver and kidney tissues were observed by hematoxylin-eosin (H&E) staining, and the apoptosis of liver and kidney tissues was observed by TUNEL staining. One-way analysis of variance was used to compare the mean values of normally distributed measurement data between groups. Comparisons between groups were performed using the least significant difference t-test. Results:The luciferase reporter gene technology showed that NFAT was significantly activated in the PQ group. After pretreatment with SKF96365, NFAT activation decreased sharply in a dose-dependent manner. HE staining showed that the outline structure of liver and kidney tissues in the PQ groups were unclear, cells swelled and a large number of inflammatory cells infiltrated; in the PQ+SKF group, liver cell swelling and inflammatory cell infiltration decreased significantly. TUNEL staining showed that the apoptotic cells in liver and kidney tissues increased in the PQ groups, and the apoptosis decreased remarkably in the PQ+SKF group.Conclusions:SOCE inhibitor SKF96365 can significantly reduce the liver and kidney injury caused by PQ.

OBJECTIVE To explore the mechanism by which gastrodin improves renal hyperten-sion in rats.METHODS A rat model of renal hypertension was established by ligating the renal artery.seventy-five rats were randomly divided into 5 groups(n=15):control group(sham operation group),model group,model+ramipril 1 mg·kg-1,model+gastrodin 100 and 200 mg·kg-1.The systolic blood pressure of the tail artery after modeling>18.12 kPa was regarded as the success of modeling.After the model was established,rats in the model+ramipril group were ig given ramipril 1 mg·kg-1 while the model+gastrodin group was ig given gastrodin 100 and 200 mg·kg-1 respectively for 4 weeks.Colori-metric assay kit was used to detect the serum superoxide dismutase(SOD)activity and malondialde-hyde(MDA)content in rats.ELISA was used to detect serum angiotensin-2(Ang-2)and aldosterone(ALD)contents,as well as serum and thoracic aortic tissue interleukin-1β(IL-1β),IL-6 and tumor necrosis factor α(TNF-α)content.HE staining was performed to detect pathological changes in thoracic aorta tissue of rats.The expressions of autophagy protein miceotubule associated protein light chain 3(LC3)-Ⅱand LC3-Ⅰwere detected by Western blotting.RESULTS The systolic pressure of the tail artery of rats after modeling exceeded 18.12 kPa,indicating that the modeling was successful.Compared with the control group,the contens of Ang-2(P<0.01)and ALD(P<0.01)in the model group were significantly increased,the activity of SOD(P<0.01)in serum and thoracic aorta tissue was significantly decreased,the content of MDA(P<0.01)was significantly increased,the contents of IL-1β,IL-6 and TNF-α in serum and thoracic aorta tissue were significantly decreased(P<0.01)and the ratio of LC-32/LC-31 in thoracic aorta tissue was significantly increased(P<0.01).Compared with the model group,gastrodin significantly increased the systolic pressure of the tail artery(P<0.01),the contents of Ang-2(P<0.01)and ALD(P<0.01)and the activity of SOD(P<0.01)in serum,as well as decreased the contents of MDA,IL-1β,IL-6 and TNF-α(P<0.01)in serum and thoracic aorta tissue.Meanwhile,gastrodin signifi-cantly decreased the ratio of LC3-Ⅱ/LC3-Ⅰ in rat thoracic aorta(P<0.01).CONCLUSION Gastrodin can improve the blood pressure of renal hypertensive rats,and the mechanism is possibly related to the reduction of autophagy protein LC3-Ⅱ/LC3-Ⅰratio.